Jillian Wise, Ph.D.
Jillian Wise, Ph.D.
Assistant Professor | Biology and Biomedical Sciences
Dr. Wise received her Ph.D in Biomedical Sciences from the University of Texas MD Anderson Cancer Center, followed by a post-doctoral fellowship at the University of Oslo in Norway. She was an Instructor at Massachusetts General Hospital of Harvard Medical School prior to her appointment at Salve Regina University. As a cross-trained computational and translational researcher, her focus is on determining mechanisms of cancer cell evolution in response to therapies in order to develop and better connect cancer patients with their most effective treatment regimens. She uses comprehensive approaches to studying evolutions of cancer cell states through in-depth genomic and transcriptomic analyses. She also focuses on developing methods of studying genomic and transcriptomic changes across evolutionary time and creating machine learning applications for cancer detection. As an educator at Salve, Dr. Wise teaches undergraduate courses on genetics and bioinformatics as well as developing future researchers in computational cancer analytics.
Featured Fall 2024
Acquired Cross-resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of MYC paralogs
Shreoshi Pal Choudhuri, Luc Girard, Jun Yi Stanley Lim, Jillian F. Wise, Braeden Freitas, Di Yang, Edmond Wong, Seth Hamilton, Victor D. Chien, Collin Gilbreath, Jun Zhong, Sarah Phat, David T. Myers, Camilla L. Christensen, Marcello Stanzione, Kwok-kin Wong, Anna F. Farago, Catherine B. Meador, Nicholas J. Dyson, Michael S. Lawrence, Sihan Wu, Benjamin J. Drapkin.
Abstract: Small cell lung cancer (SCLC) presents as a highly chemosensitive malignancy but acquires cross-resistance after relapse. This transformation is nearly inevitable in patients but has been difficult to capture in laboratory models. Here we present a pre-clinical system that recapitulates acquired cross-resistance in SCLC, developed from 51 patient-derived xenografts (PDXs). Each model was tested for in vivo sensitivity to three clinical regimens: cisplatin plus etoposide, olaparib plus temozolomide, and topotecan. These functional profiles captured hallmark clinical features, such as the emergence of treatment-refractory disease after early relapse. Serially derived PDX models from the same patient revealed that cross-resistance was acquired through a MYC amplification on extrachromosomal DNA (ecDNA). Genomic and transcriptional profiles of the full PDX panel revealed that this was not unique to one patient, as MYC paralog amplifications on ecDNAs were recurrent among cross-resistant models derived from patients after relapse. We conclude that ecDNAs with MYC paralogs are recurrent drivers of cross-resistance in SCLC.
Access:
Cancer Discovery, February 2024
Open Access: DOI 10.1158/2159-8290.CD-23-0656